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Pancreatic Neoplasms: HELP
Articles by Ulf Geumann
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Ulf Geumann wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Multiplexed pancreatic genome engineering and cancer induction by transfection-based CRISPR/Cas9 delivery in mice. 2016

Maresch, Roman / Mueller, Sebastian / Veltkamp, Christian / Öllinger, Rupert / Friedrich, Mathias / Heid, Irina / Steiger, Katja / Weber, Julia / Engleitner, Thomas / Barenboim, Maxim / Klein, Sabine / Louzada, Sandra / Banerjee, Ruby / Strong, Alexander / Stauber, Teresa / Gross, Nina / Geumann, Ulf / Lange, Sebastian / Ringelhan, Marc / Varela, Ignacio / Unger, Kristian / Yang, Fengtang / Schmid, Roland M / Vassiliou, George S / Braren, Rickmer / Schneider, Günter / Heikenwalder, Mathias / Bradley, Allan / Saur, Dieter / Rad, Roland. ·Department of Medicine II, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany. · German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. · Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. · Institute of Radiology, Klinikum rechts der Isar, Technischen Universität München, 81675 Munich, Germany. · Department of Pathology, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany. · Institute of Virology, Technische Universität München/Helmholtz Zentrum München, 81675 Munich, Germany. · Instituto de Biomedicina y Biotecnología de Cantabria, 39011 Santander, Spain. · Helmholtz Zentrum München, Research Unit Radiation Cytogenetics, 85764 Neuherberg, Germany. · Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ·Nat Commun · Pubmed #26916719.

ABSTRACT: Mouse transgenesis has provided fundamental insights into pancreatic cancer, but is limited by the long duration of allele/model generation. Here we show transfection-based multiplexed delivery of CRISPR/Cas9 to the pancreas of adult mice, allowing simultaneous editing of multiple gene sets in individual cells. We use the method to induce pancreatic cancer and exploit CRISPR/Cas9 mutational signatures for phylogenetic tracking of metastatic disease. Our results demonstrate that CRISPR/Cas9-multiplexing enables key applications, such as combinatorial gene-network analysis, in vivo synthetic lethality screening and chromosome engineering. Negative-selection screening in the pancreas using multiplexed-CRISPR/Cas9 confirms the vulnerability of pancreatic cells to Brca2-inactivation in a Kras-mutant context. We also demonstrate modelling of chromosomal deletions and targeted somatic engineering of inter-chromosomal translocations, offering multifaceted opportunities to study complex structural variation, a hallmark of pancreatic cancer. The low-frequency mosaic pattern of transfection-based CRISPR/Cas9 delivery faithfully recapitulates the stochastic nature of human tumorigenesis, supporting wide applicability for biological/preclinical research.

2 Article A conditional piggyBac transposition system for genetic screening in mice identifies oncogenic networks in pancreatic cancer. 2015

Rad, Roland / Rad, Lena / Wang, Wei / Strong, Alexander / Ponstingl, Hannes / Bronner, Iraad F / Mayho, Matthew / Steiger, Katja / Weber, Julia / Hieber, Maren / Veltkamp, Christian / Eser, Stefan / Geumann, Ulf / Öllinger, Rupert / Zukowska, Magdalena / Barenboim, Maxim / Maresch, Roman / Cadiñanos, Juan / Friedrich, Mathias / Varela, Ignacio / Constantino-Casas, Fernando / Sarver, Aaron / Ten Hoeve, Jelle / Prosser, Haydn / Seidler, Barbara / Bauer, Judith / Heikenwälder, Mathias / Metzakopian, Emmanouil / Krug, Anne / Ehmer, Ursula / Schneider, Günter / Knösel, Thomas / Rümmele, Petra / Aust, Daniela / Grützmann, Robert / Pilarsky, Christian / Ning, Zemin / Wessels, Lodewyk / Schmid, Roland M / Quail, Michael A / Vassiliou, George / Esposito, Irene / Liu, Pentao / Saur, Dieter / Bradley, Allan. ·1] Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, München, Germany. [2] German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany. [3] The Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridgeshire, UK. · The Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cambridgeshire, UK. · Department of Pathology, Klinikum Rechts der Isar, Technische Universität München, München, Germany. · 1] Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, München, Germany. [2] German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Medicine II, Klinikum Rechts der Isar, Technische Universität München, München, Germany. · Instituto de Medicina Oncológica y Molecular de Asturias (IMOMA), Oviedo, Spain. · Instituto de Biomedicina y Biotecnología de Cantabria (UC-CSIC-SODERCAN), Santander, Spain. · Department of Veterinary Medicine, University of Cambridge, Cambridge, UK. · Biostatistics and Bioinformatics Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA. · Bioinformatics and Statistics, The Netherlands Cancer Institute, Amsterdam, the Netherlands. · Institute of Virology, Technische Universität München, Munich, Germany. · Institute of Pathology, Ludwig Maximilians Universität München, München, Germany. · Institute of Pathology, Universität Regensburg, Regensburg, Germany. · Institute of Pathology, Technische Universität Dresden, Dresden, Germany. · Department of Surgery, Technische Universität Dresden, Dresden, Germany. · Institute of Pathology, Medizinische Universität Insbruck, Insbruck, Austria. ·Nat Genet · Pubmed #25485836.

ABSTRACT: Here we describe a conditional piggyBac transposition system in mice and report the discovery of large sets of new cancer genes through a pancreatic insertional mutagenesis screen. We identify Foxp1 as an oncogenic transcription factor that drives pancreatic cancer invasion and spread in a mouse model and correlates with lymph node metastasis in human patients with pancreatic cancer. The propensity of piggyBac for open chromatin also enabled genome-wide screening for cancer-relevant noncoding DNA, which pinpointed a Cdkn2a cis-regulatory region. Histologically, we observed different tumor subentities and discovered associated genetic events, including Fign insertions in hepatoid pancreatic cancer. Our studies demonstrate the power of genetic screening to discover cancer drivers that are difficult to identify by other approaches to cancer genome analysis, such as downstream targets of commonly mutated human cancer genes. These piggyBac resources are universally applicable in any tissue context and provide unique experimental access to the genetic complexity of cancer.